fig1

Figure 1. A model for BRD4-induced diastolic dysfunction in COVID-19 patients. A cytokine storm elicited by SARS-CoV-2 infection triggers phosphorylation and activation of BRD4, resulting in changes in gene expression that culminate in diastolic dysfunction. BET inhibitors prevent the binding of BRD4 to acetyl-histones in chromatin, thereby preventing cytokine storm-driven diastolic dysfunction. BRD4: Bromodomain-containing protein 4; BET: bromodomain and extra-terminal.